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The primary care approach

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1 The primary care approach
Proteinuria The primary care approach Presented by feras ghosheh 6th Y medical student AL-QUDS UNIVERSITY


3 INTRODUCTION The protein is found in normal urine, and it’s divided into: 1-60% plasma proteins: albumin (major) IgG, IgA ,light chains ,heavy chains , transferrin ,haptoglobin ,lysozyme ,amylaze ,kallikrein. 2- 40% originating from the secretions of the urinary tract including: tamm-horstall ,urokinase and secertory IgA. The reasonable upper limit of normal protien excretion in healthy children = 150 mg/24 hrs.

4 DEFINITION The excretion of an excessive amount of protein (>150mg/day) in the urine as defined by qualitative, semi-quantitative, and quantitative methods.

5 EPIDEMIOLOGY incidence: 1 - 5% (depend upon age and number of samples) prevalence: % (1+ proteinuria) only 10% of kids with proteinuria will have abnormalities after 6-10 month of follow-up of those children with isolated proteinuria, <2% will have significant underlying renal disease the incidence of proteinuria in patients with underlying renal disease is remarkably high

6 There are three basic types of proteinuria :
PATHOGENESIS There are three basic types of proteinuria : 1-glomerular 2-tubular 3- overflow

7 1. Glomerular mechanisms: proteins: larger macromolecules, albumin
. increased GFR . increased glomerular permeability basement membrane endothelial, epithelial cell injury electrostatic charge barrier proteins: larger macromolecules, albumin

8 2. Tubulointerstitial impaired tubular reabsorption of filtered proteins proteins: low MW proteins, lysozyme, B2-microglobulin Tamm-Horstall protein

9 3. Overload Proteinuria increased load overloads tubular reabsorptive capacity proteins: low MW plasma proteins, Ig light chains, myoglobulin, lysozyme, albumin

10 1. Benign Proteinuria a. Benign Transient Proteinuria
b. Orthostatic Proteinuria c. Persistent Asymptomatic Proteinuria

11 2. Pathologic Proteinuria
A- Glomerular 1. Hereditary 2. Non-Hereditary B-Tubulointerstitial

12 A- Glomerular 2. Chronic Acute (GN) 1. Hereditary 1. Primary
Minimal Change Disease* FSGN Mesangioproliferative GN Membranous GN Membranoproliferative GN 2. Secondary Berger (IgA) Nephropathy Goodpastures Nephropathy SLE Nephropathy Wegeners Nephropathy Diabetic Nephropathy Renal Vein Thrombosis Sickle Cell Disease 1. Hereditary Congenital Nephrotic Syndrome Alport Syndrome 2. Non-hereditary Acute (GN) -Poststrep GN -H.U.Syndrome -H.S. Purpura

13 B-Tubulointerstitial
2. Non-Hereditary Acute Tubular Necrosis analgesic abuse antibiotics cystic diseases heavy metal poisoning homograft rejection hypokalemia interstitial nephritis penicillamine reflux 1.Hereditary Cystinosis Galactosemia Lowe Syndrome Medullary Cystic Kidney Proximal RTA Wilson Disease

14 3. Overload Proteinuria 1. Neoplastic 2. Others Amyloidosis
Leukemia (monocytic, monomyelocytic) - lysozymuria Multiple Myeloma Waldenstrom's Macroglobinemia 2. Others IDDM (microalbuminuria) repeated albumin or blood transfusions Rhabdomyolysis most common causes of proteinuria in childhood

15 CLINICAL FEATURES: 1. History of Presenting Illness
at the end of the history, one should be able to discern: 1. benign vs pathologic proteinuria (if pathologic then) 2. glomerular vs tubulointerstitial proteinuria (if glomerular then) 3. hereditary vs non-hereditary (if non-hereditary then) 4. acute GN vs chronic GN (if chronic then) 5. primary GN vs secondary GN 6. nephrotic vs non-nephrotic proteinuria 7. proteinuria with or without hematuriauria onset when began with conditions identified around the initial presentation, i.e., drug ingestion record of previous urinalyses precipitation/palliation identification of triggering agents infectious, drugs, foods, chemicals, vaccinations helps to identify acquired forms of tubulointerstitial proteinuria

16 associated with hematuria severity
quality associated with hematuria severity more likely to be pathologic proteinuria if associated with hematuria or Nephrotic Syndrome (edema, hypoalbuminemia, hypercholesterolemia) if Nephrotic Syndrome present: likely to be a primary GN unlikely to be benign etiology or secondary GN timing acute vs acute-on-chronic intermittent vs persistent duration of proteinuria associated symptoms past medical history functional inquiry helps to differentiate acute GN from chronic GN helps to identify overload proteinuria causes

17 Family History helps to differentiate hereditary from non-hereditary forms of both glomerular and tubulointerstitial forms of proteinuria: 1. Proteinuria family members must have had previous urinalysis to ascertain this 2. Renal Disease Polycystic Kidney Disease Nephrotic Syndrome, Fanconi Disease renal dialysis kidney transplantation 3. Others hearing/ocular impairment (Alport Syndrome)

18 Specific Entities 1. Benign Transient Proteinuria
benign proteinuria associated with precipitating factors - fever, exercise, stress, cold weather, dehydration, high blood pressure, seizures, etc Orthostatic Proteinuria2. diagnosis based upon the Postural Test has a benign clinical course

19 3. Persistent Asymptomatic Proteinuria
proteinuria that persists for 3-6 months renal biopsy after 6 months of persistent proteinuria and if FSGS then at risk for chronic renal failure 4. Congenital Nephrotic Syndrome onset at birth with Nephrotic Syndrome (massive proteinuria, hypoalbuminemia, edema, and hyperlipidemia) very difficult to treat with poor prognosis 5. Poststreptococcal GN proteinuria + hematuria associated symptoms prodrome of pharyngitis, URTI, impetigo Nephrotic and/or Nephritic Syndrome

20 6. Hemolytic Uremic Syndrome proteinuria + hematuria
associated symptoms prodrome of bloody diarrhea anemia and thrombocytopenia (petechiae) Nephrotic and/or Nephritic Syndrome 7. Henoch-Schoenlein Purpura purpuric rash, arthritis, abdominal pain 8. Primary Glomerulonephritis isolated proteinuria +/- Nephrotic Syndrome edema, hypoalbuminemia, hyperlipidemia

21 9. Secondary Glomerulonephritis
proteinuria +/- hematuria associated with a disease entity, i.e., SLE, Goodpastures Disease, Wegeners Disease, Diabetes Mellitus 10. Hereditary Tubulointerstitial Proteinurias tubular proteinuria associated symptoms episodes of vomiting, dehydration, weakness, fever, anorexia, constipation, failure to thrive, polydipsia, polyuria

22 INVESTIGATIONS 1. Proteinuria (Diagnosis) 1. Qualitative - Dipstick
measures a range of protein concentrations depth of colour increases in a semiquantitative manner with increasing urinary protein concentration to rule out false positives must have: 3 samples with proteinuria first voided early morning samples pH < 6.0 with known specific gravity 1+ ( mg/24 hrs) or greater is considered abnormal dependent on specific gravity of urine sample FP: gross hematuria, highly alkaline urine, UTI

23 2. Semi-quantitative - Protein/Creatinine Ratio in Urine
random early morning single voided specimen children < 2 years : < 0.5 children > 2 years : < 0.2 nephrotic : > 3.5 correlates with the 24 hour protein excretion data

24 3. Quantitative - 24 hr. urine collection
gold standard if dipstick is 1+ or more than obliged to do a 24 hour urine collection 24 hr. urine collection Protein (mg)/m2/hr < 4 mg/m2/hourr (normal) 4-40mg/m2/hour (proteinuria) 40 mg/m2/hour (nephrotic) Protein (mg)/24 hr 2 to 12 months : > 155 mg/24 hr 3 to 4 years : > 140 mg/24 hr 4 to 10 years : > 190 mg/24 hr 10 to 16 years : > 250 mg/24 hr FP: radiographic contrast media, cephalosporins, pencillin analogues, sulfonamide metabolites

25 2. Indications for Further Investigation
Non-orthostatic Proteinuria Persistent Proteinuria Symptomatic (edema, elevated BP, abdominal pain, hematuria)

26 3. First Line Investigations
1. Urinalysis R&M, C&S, microscopy orthostatic test 24 hour collection total protein creatinine clearance 2. Serum electrolytes, BUN, creatinine, albumin, cholesterol, triglyceride, calcium, protein, CBC 4. Second Line Investigations 1. Urine protein electrophoresis can be used to differentiate glomerular (albumin) from tubular (Tamm-Horstall) proteinuria 2. Serum IgA, PTH, ANA, protein electrophoresis, ASOT, anti-GBM antibodies, uric acid, C3, C4 3. Imaging Studies renal ultrasound to rule out renal vein thrombosis 4. Renal Biopsy indicated for: progressive proteinuria with hematuria all forms of Nephrotic Syndrome except that caused by steroid-responsive Minimal Change Disease

27 MANAGEMENT treat underlying disorder treat complications

28 Thank you

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